Thursday, August 30, 2018

Article: Nutrigenomics and the Future of Nutrition: Proceedings of a Workshop

 https://www.ncbi.nlm.nih.gov/books/NBK518615/


Quoted article summary: 

BOX 3-1Overview of Points Presented by Individual Speakers

  • In contrast to the wellness industry, which has a mixed reputation because of the many non-scientifically based approaches being applied, the goal of “scientific wellness” is to provide an underpinning of rigorous science and dense, dynamic data for the study of wellness, and to predict and prevent disease before it happens. To launch scientific wellness, the 100K Wellness Project was conceived, focused on collecting a personal, dense, dynamic dataset for 100,000 individuals that can be observed over time for early warning signs of disease. (Price)
  • Meanwhile, a 9-month feasibility study, the Pioneer 100 Wellness Project, has demonstrated improvements in a number of clinical markers. Along with data collection, wellness coaching was an important part of the study, reflecting the critical role of behavior change in personalized nutrition. (Price)
  • Research has explained arginine deficiency syndromes, mostly in relation to sickle cell disease, an autosomal recessive inherited disease, but also trauma. Both have distinct nutritional requirements that develop because of metabolic abnormalities, and both may benefit from arginine replacement therapy. (Morris)
  • Although the potential benefit of arginine therapy for sickle cell disease, as well as for trauma, has been demonstrated in both mice and humans, most of these studies are limited by methodological weaknesses. More research is needed, including the identification of subpopulations that would likely benefit the most from arginine replacement therapy. (Morris)
  • Nutrigenomic studies are difficult not only because they are complex, but also because proving causation from association is especially challenging in the field of nutrition. Additionally, except for diseases caused by single gene defects, it is very difficult to isolate which components of a disease phenotype are related to nutrition. (Alpers)
  • Because of these difficulties, many scientific approaches to studying links between genomics and nutritional phenotypes have relied on in vitro and in vivo animal studies. A long lag time can be expected before strong human data are available and nutrigenomics can be commercially implemented. (Alpers)
  • Evidence from studies on the CYP1A2 genotype and coffee intake are “proof of concept” that a single nucleotide polymorphism (SNP) can modify the association between a dietary component and a variety of different health outcomes. (El-Sohemy)
  • There are problems with the ways in which nutrigenomics is portrayed in the media and information about the field is communicated. An example is an article in which a pediatrician who was interviewed said he was unaware of evidence suggesting that people with different FTO gene variants respond differently to low-protein versus high-protein diets. Yet not only does such evidence exist, but it has been replicated. (El-Sohemy)
*

This list is the rapporteur's summary of the main points made by individual speakers (noted in parentheses). The statements have not been endorsed or verified by the National Academies of Sciences, Engineering, and Medicine, and they are not intended to reflect a consensus among workshop participants.

From: 3, Personalized Nutrition in the Real World

Cover of Nutrigenomics and the Future of Nutrition
Nutrigenomics and the Future of Nutrition: Proceedings of a Workshop.
National Academies of Sciences, Engineering, and Medicine; Health and Medicine Division; Food and Nutrition Board; Food Forum.
Washington (DC): National Academies Press (US); 2018 Jul 25.

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